Diabetes is one of the most common metabolic disorders in humans. Indeed, nearly 1 million Americans are afflicted with juvenile-onset diabetes. This form of the disease is also known as insulin-dependent or Type I diabetes, and usually appears abruptly during childhood or young adulthood. Type II, or non-insulin-dependent diabetes is characterized by a less abrupt onset. Type II diabetes commonly occurs beyond the age of 40 or so. Both types of diabetes impair the body's ability to access blood glucose for use as an energy source. Chronically high levels of blood sugar gradually damage many tissues and organs of the body.
Substantial efforts have been directed toward understanding the causes and consequences of diabetes. A strong autoimmune component is now believed important in the etiology of type I diabetes (see Science 225:1381 (1984), and Immunology Today 5:230 (1984)). The metabolic consequences of experimentally induced diabetes have also been explored. For example, in Diabetes 31:426 (1982) Schneir et al. demonstrated that collagen, an important structural protein of skin, has a significantly decreased half-life in diabetic rats. It is well appreciated that both forms of diabetes impact the tissues of the body in a global fashion.
Despite the availability of insulin treatment, diabetes remains a serious disease that is responsible for many deaths and substantial morbidity worldwide. For example, the life-span of the average diabetic is shortened by as much as 50%. Although insulin treatment can assist in regulating blood sugar levels, the degree of this control is typically insufficient to prevent many of the sequelae from diabetes. The consequences from long term diabetes can include eye damage, often leading to blindness; circulatory problems; problems with wound healing; and other serious consequences. Improved treatments for diabetes are urgently required.